Liver Flashcards
no invasive
Ultra
elastormetry
ct
semiinvasiev
cholecustocholangiography
ercp-endoscopic retrograde choalngiopankreticography
acute liver injury non specooc enzymes
ALT, AST
chonic liver ezyme
GMt-glutamyltranferase
oncomakekers
AFP by hepatocellular carcinoma
CEA(carcinoembryonal antigen) by cholangiocellular ca
INASIVE
ANGIOGRAPHY
LIVER NIPSY
developmental abnormalities of over
-common, not serois
1.liver cyst
2. congenital heptic fibrosis
liver/bilary cyst
-AD
-bile duct dilation is reason
POLYCYSTIC liver disease
-AD-
-ADPKD
-cyst in pancrea, spleen, oavries, ling
-ALLTID OF KIDNEY OGSP
congentialheptic fibrosis
-AR
-PORTAL HYPERTENSION
-fucntion normla
Inborn metabolic diases
-tesaurismoses
-deficinecy of a1-antitrypsin
-def of a1-antichymotrypsin
-fibrin storage disease
tesaursismoses
storage disorder
.amyloidosis, lipidoses, glykogenosis
deficiency of a1 antitrypsin
-AR
-hepatitis, choelstasis, fibrosis/cirrhoiss
-lung ephysmea+resp fialureee
Inbron metabolic lover disease
Wilson disease
porphyria
IRON: inborn haemochromatosis and haemosiderosis
wilson
-damaged liver + iris/lens
-acc of copper
-normal: rabsorption of copper from intestine –>by albumin–>liver tissue and then by cerruplasmin to stool
-cerruplasmin dont work
-Liver injury: ACUTE lover failure, haemolytic aneima w kindey filure, chronic liver disease->fibrosis/cirrhosis
brian
irisl/lens_->kayser-fleischers ring
porphyria
hepatic:
-inborn
-acquired(80%): alchol, HIV, msoking,
erythropoeitic
clinic:liver injurt and sking signs:blister/erythema
- photodermatoses
-acc of uv light
haemochromatosis
-AR
- eat–>^abs or iron from intesitines–>overload–>iron acc in liver and so on
-BRONZE DIABETES: cirrhosis+DM+skin pigmetation
congetial
kupher cells
ACC MAINLY IN HEPTOCYTES
haemosiderosis
-ext/int ron overload
types
1. internal bc of hemolysis
2.external: alcholo, repeted blood transfusuin
typucally reversible
NOT inhertited obvi
Kupcher cells
ACC OF IRON MAINLY IN MACROPHAGES/KUPFER
toxic liver isease
-alco and drugs
- Intrinsic=predicitible
-^durgs=înjury
-serious ness depent of dose
-know durg and tocins
-direct=injury of heptocytes
-indirtc=incorporation into metabolism
-quick symtoms - idosyncratic=unpredictable
-individual dororder of metabolsim of toxin/interaction w immune
-toxin ecssesd base dose=NOT DOSE DEPENDANT
-d,w,month for clinical manifestaiton
liver injuty:
-ACUTE HEPATITIS, chronic, csteatosis, fibrosis, choelstssis, GRANULOMATOUS
Steatosis
calssifiction
-AFLD:alcoholic fatty liver disease
-NAFLD
etiology of NAFLD
- obestity, DM, hyeprlidpidemina, tocins, durgs, hepttis, meta liver disease
LARGE LIVER, SOFT, YELLOW
Chronic liver venous steasiss/hyperemia
Chronic hepatic venous stasis is a manifestation of long-term venous hyperemia in chronic venous liver disease right heart failur
Macroscopically has an image of the nutmeg liver - hepar moschatum
Cyanotic induration of the liver is also accompanied by chronic venostasis of the spleen and kidneys
Necrosis in zone 3(around central vein)(hyperemia), steatosis more peripherally(around the CENTRILOBULAR veins)
Shows increase amount of collagen and reticular fibers around the central veins (so-called “cardiac fibrosis”)
alchol injury liver
-most common
-injurt: stetosis, steotheptitis, cirr, fibro, choelstatsis
HARD
acute hepatitis
-acute injury +NECROSIS
-is reverrsibøe, regenreraiton can happens
-SELF limiting
-flu, jaundive, nasue, abd pain, heptomegalu
-asymptoamtic
NO FIBROOS-so therefore NO CIRRHOSIS HAPPENING
chronic heptitis
-persisent
-chornic infla of protal tract+parenchymal infla+fibrosis–>cirhosis
->6monts
hepatotorphic viruses
HAV, HBV,C,D,E
Accompaniying heptis
herpes, adenoviruses, CMV, EBV
unifectious heptotis
acute choelstiss, durg, autoimmune, alcholl injury
serousness of acute heptitis
amount of necrosis
cyryptogenous hepatitis
unknown etiology
acute viral heptotis according to type of virys
DNA: bare HBV
resten RNA
acute viral heptotis according to INCUBATION
hav: 3-6 w
hbv:1-6m
hcv:15-150days
acute viral heptotis according to transtition
F-O route: A OG E
resten parenteral
acute viral heptotis according to chronic hepatitis
NO: A OG E
retsen JA
Worl most common HV
HBV
sex, no gloves, nlood transfusion
most common in europe
HCV- no vacciantion
most common in slovakia
HAV: dirty hands
acute viral heptitic
Most common is subclinical(60%) and acute hepatits(25%)
most common and mostly cured-60-90%
acute viral hepatitis C
least comon, more severe
-chronic hepatitic (85%%)
B and C contribuye to
heaptocellular caricnoma
acute viral hepatitis D
-incomplete viral particle
-need B for replicaiton
-WORST DIAGNOSIS
- confection:HBV+HDV: most cured w no consequence
- superinfect HDV : chronic B virus+new D virus infection–>chornicn hepatitis -70-80%
chronci viral hepatitis-grading anstaging
garding-grade of activity aka extend of necrosis and infla infiltrate
staging-stage of disease aka amoth og fibrosis and cirrhosis
choelssrtasis
-acc of bile in body
complete: both bile and salt=>ICTERUS
incomplete: no biliruben, bare BA+SALT
intrahepatal7extahepatal
CLINICAL:
-Yellow color os skina dn scleras: complete
-dark urine + alcholoc stool
-skin itching
icterus-jaundice
-acc of biirubin +BA in body
-un
1.hemolytic/preheptic:
-ûrobilinogen
- hepatocellualr icterus
^conjuagted, biles salt
âst, alt - choelstatic icterus:
-disorder of bielexcretion
-CLAY colored stool
-^conjuagted+bile salt
primary bilairy cirrhosos(cholangitis)
aff bile dcuts w/o hepatocyte injury
-intra
Probably of Autoimmune origin - amboss says it is has autoimmune origin
primary scleorising cholangitis
aff bile ducts W hepatocyte injury
secondayr scelrosing cholangitis
known etio
after surgery, choelslithiasis, infection, inborn, isnchemic biel ducts
obstruction of extrahepatal bile ducts-gallstone
-mostt common
gallstone
neoplasmi
strictures
PSC
atresis
parasitic
purulent cholangitis
-bacteri go for inetsine up into bile duct–>infla–>pus
-reason bile duct obstruction
-ascendent spread for extraheptic biliary tract
complication:rupture, abscess, postinfla stenoses
liver absecc
-localizeed purulent infla of liver
- MTS by lump or vv by purulent ifn of GIT
parasitic infections of liver
-echinnococus granulosos
-infl of intestines
-dogs/foc->humans
cyst development filled w infectius agenst called scotex
vascular disease of liver
acute arterial blockage
closuer of heptoc veins
ACUTE BLOCAGE OF INTRAHEPATIC BRANCHE SOF PROTAL VEINS
CHORNIC LIVER VENOSTASIS
acute arterial bloacge
of hepatic a–>necrosis
-smaller–>w/o injury bc anastomose
closure of hepatic veins
-ACUTE BUDD CHIARI SYNDROME(acute stasis of blood in liver–>enlargemed))
-pyelephlebitis, tumors
-hypercoagualitve conditions, aucte liver fialure, haemorrahic inftction of intesine
chornic budd chiary syndri
-post infla stenosis of veins
-thromboses
-cardic disease=HF
Budd chiari syndrome is a post-hepatic and intra-hepatic cause of portal hypertension
SCUTE BLOCAGE OF INTRAHEPTIC BRANCHES OF PORTAL VEINS
-NO necrosis
-pale/congested
-lievr cells alive
chonic liver venostais
-CYANOTIC INDURATION OF LIVER=NUTMEG
symttoms:
-heptomegaly, ascites, jaundince, fatigue, cardial cirrhosis
etiology:
RHFFFFFF, chronic budd chiari
liver cirrhossi
final cons of chronic liver injury
classificaiton
-micronodualr: <3mm, macro >3mm, bilaru
-result: liverfaiulre + portal hypertension
liver nelarged but afuncitonal
micro:
-uniform zise and snamll
-most common of cirrhosis
-chronic injury
macro:
-irr size of noduls
-potato
- after acute necroiss
-patocytes abnormal arrangment
bILIARY:
-MICRONODULAR +DISTINH CHOLESTSIS
-BILE DUCT INJURT
-YELLOW/GREN
PORTAL HYPERTENSION
^pressure of bllod in hepatic porta–>problem leaving thorugh liver and is acc in abd cavity
site of blockage
1.prehepatal:
-blockage of protal veins
-MPN, hypercoagulaiton
- intahepatal:
-most common
-cirrhosis, fibrosis,venoocclusive disease - post hepatal:
-heptic veins–>vena cava
-budd chiari
-mpn, pregnancy, constrictive pericarditis
rsult:
-collaterals
- splenomegaly+hypersplenism+ascites
compli:
eso varices bleeding and gaemorrodes
hypocoagulaion state
hepatal failuremclinical
encephalopathy
haemorragic diatesis: dec coagualtion facots
icterus
hypaalbunemy, oedema
arterial hypotension
renal failure
hypoventilation
hormonal dosrpder:gynecomastia, vascualr spiders, female escutcheon, testicular atrophy
compliction f liver failure
brain edema, bleeding into GIT by varieses, hypoglycemy, heptorenal failure, sepsis
being tumor of liver
-not comon
1. focal nodular hyperplasa
-patho blood supply
-pver prolif of parenchyme
-not ture. pseudotumorus
- hepatocellualr adenoma
-TRUE BEING
-women yougn
- estrogen and corticoids
3.hemangioma: MOST COMMON, TRUE BEING
most common malignatn tumor of liver
HEPATOCELLULAR CARCINOMA
-aplpha fetoprotein
etiology: alfatoxine, acohol chronic hepatitis, oral contrceptivem smokin, chronic metabolic disease
-aplhatocin+HBV
clincial: abd pain+discomfort, hepatomegaly, veingt loss, cirrhosis deompensaiton
MTS: liver, lung,LN
most common malignnt ymor in chilhoord
hepatoblastoma
- solitay
-no cirrhosis
-MTS:lung and brains
inheriteed abnormalitis of gallbaldder and bile ducts
stenosis or atresia of ectraheptic bile ducts
abnormalitis of cyst duct+anomlies of blood supply
othe rmalingnt tumor
cholangiocellualr caricnoma
-chronic infla bile duct disease
-tumor of white color, not weel demercated, macro dsitint infiltartove growth
cholecystolithasis
most common affecting gallbaldder
etio: chole strones, pigment sotnes-haemolysis, alchohol, cirrhosis, 4XF rule
complication: cholcystitis
clincial:
-asym
- subcostal reion pain
-no fatty food
cholesterolosis
common lesion w no clinical imoact
acc of chol crystls in mucosa–>white/yellow
-STRAWBERRY GALL
acute choelcysttitis
-acutye infla of bile sac
-95% accompaniend by choleites
clincial: right ypper quadrant pain, tenderness, fever
complicaiton: ascending extra or intarheptic choalngitis, gallbladder emphysema, liver abscess, rupture–>peritonints, fistulation
chronci cholecystits
-acc omapnied by cholelites
clinical: abd discomfort/pain after fodd
complication: porcelian gallbrllader, mucocela, carcinoma
malignant utmor og gallbladder
-main risk factor: cholecystolithiass
ADENOCARCINOMA OF GALLBALDDER
-female
- etiologt: stone, often chron infla
clinical’: silent and unsepcific,a bd pain, weight loss, fever, jaundice, cholestasis
being tumor og gall
-cholesterol polyps
-adenomatous hyperplasoa: fundus of gall, dilation of glands+smooth m prolif, not ture
-adneoma of gallbladder:pyloric gland/intestinal, ture
most imp inborn disease of pancreas
mucoviscidosis/cystic fibrosis
-AR inherited
-production of thick mucus everywhere in body–>multiorgan consequence
acute pancreatitis-etio and pathogenesis
etiologt:
-mechnaical:bile stones, tumor, duodenal stenossi
-toxi: alcohol
-trauma:abd truam, operaiton
-iscehmic
-idiopathic
pathogeneis:
act of proenzymes by regurgaitaiton of duodenal content–>tissue autodigesiton by yrypis–»act of resting snzymes
acute pancreatitis-types, clinical, complicaiotn
types:
- acute intestitial pancratitis-NO NECROSIS, odema, infl, tissue injurt, ALCHO ABUSE,
-acute hemmorgahic/necrotixin
clinic
-acute abd pain, nause, vomiting, meteorism
complic:
- pancretic abscess–>pseudocyst–>duo obstruciton
-spesi, abscess, DIC, shock(ARDS),a cute renal failure, bleeding in git, thromboses
chronic pancretitis
-alchol mostlyyyy
-stones
-genetic
-autoimmuinue
-idiotpathi
clincial: abd pain, inotlerance to food
complicaiton: maldigestion, dm , acute appendicits
most common and most aggresive tumor of pancrea
ductal pancreatic carcinoma
etio:
hereditaru, chronic pancreatitis, dm, smokin
clinical:
-silent, epiagstric pain, weight loss, icterus
other pancreatic tumors
1.acinar adenocarcinoma
-5y survival 6&
- nerudndocrine neoplasme
-hormonally active - pancreatoblastoma-rare
- in childhood
-50% curability
